A3 receptor agonist modulates IL-1β hippocampus levels in a rat model of neuropathic pain
Autor(a) principal: | |
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Data de Publicação: | 2022 |
Outros Autores: | , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UFRGS |
Texto Completo: | http://hdl.handle.net/10183/250315 |
Resumo: | Introduction: Considering the lack of specific treatments for neuropathic pain, this study aimed to evaluate the effect of a single dose of adenosine A3 receptor IB-MECA on inflammatory and neurotrophic parameters in rats subjected to a neuropathic pain model. Methods: 64 adult male Wistar rats were used. Neuropathic pain was induced by chronic constriction injury (CCI) of the sciatic nerve and the treatment consisted of a 0.5 μmol/kg dose of IB-MECA, a selective A3 adenosine receptor agonist, dissolved in 3% DMSO; vehicle groups received DMSO 3% in saline solution, and morphine groups received 5 mg/kg. Cerebral cortex and hippocampus IL-1β, BDNF, and NGF levels were determined by Enzyme-Linked Immunosorbent assay. Results: The main outcome was that a single dose of IB-MECA was able to modulate the IL-1β hippocampal levels in neuropathic pain induced by CCI and the DMSO increased IL-1β and NGF hippocampal levels in sham-operated rats. However, we did not observe this effect when the DMSO was used as vehicle for IB-MECA, indicating that IB-MECA was able to prevent the effect of DMSO. Conclusions: Considering that the IL-1β role in neuropathic pain and the contributions of the hippocampus are well explored, our result corroborates the relationship between the A3 receptor and the process of chronic pain maintenance. |
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Cioato, Stefania GiottiMedeiros, Liciane FernandesLopes, Bettega CostaMedeiros, Helouise RichardtCaumo, WolneiRoesler, RafaelTorres, Iraci Lucena da Silva2022-10-26T04:47:33Z20222357-9730http://hdl.handle.net/10183/250315001148411Introduction: Considering the lack of specific treatments for neuropathic pain, this study aimed to evaluate the effect of a single dose of adenosine A3 receptor IB-MECA on inflammatory and neurotrophic parameters in rats subjected to a neuropathic pain model. Methods: 64 adult male Wistar rats were used. Neuropathic pain was induced by chronic constriction injury (CCI) of the sciatic nerve and the treatment consisted of a 0.5 μmol/kg dose of IB-MECA, a selective A3 adenosine receptor agonist, dissolved in 3% DMSO; vehicle groups received DMSO 3% in saline solution, and morphine groups received 5 mg/kg. Cerebral cortex and hippocampus IL-1β, BDNF, and NGF levels were determined by Enzyme-Linked Immunosorbent assay. Results: The main outcome was that a single dose of IB-MECA was able to modulate the IL-1β hippocampal levels in neuropathic pain induced by CCI and the DMSO increased IL-1β and NGF hippocampal levels in sham-operated rats. However, we did not observe this effect when the DMSO was used as vehicle for IB-MECA, indicating that IB-MECA was able to prevent the effect of DMSO. Conclusions: Considering that the IL-1β role in neuropathic pain and the contributions of the hippocampus are well explored, our result corroborates the relationship between the A3 receptor and the process of chronic pain maintenance.application/pdfengClinical and biomedical research. Porto Alegre. Vol. 42, no. 2 (2022), p. 128-134Receptor A3 de adenosinaCitocinasDimetil sulfóxidoNeuralgiaFatores de crescimento neuralRatosAdenosine A3 receptorCytokineDMSON6-(3-iodobenzyl) adenosine-5’-methyluronamide (IB-MECA)Neuropathic painNeurotrophinRatsA3 receptor agonist modulates IL-1β hippocampus levels in a rat model of neuropathic paininfo:eu-repo/semantics/articleinfo:eu-repo/semantics/otherinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSTEXT001148411.pdf.txt001148411.pdf.txtExtracted Texttext/plain31678http://www.lume.ufrgs.br/bitstream/10183/250315/2/001148411.pdf.txt34c37881b3e26696af3bbc7e4d49f28eMD52ORIGINAL001148411.pdfTexto completo (inglês)application/pdf1213607http://www.lume.ufrgs.br/bitstream/10183/250315/1/001148411.pdfeaaa3c5f1108179ac797024aa32d70fbMD5110183/2503152023-01-14 06:14:46.101938oai:www.lume.ufrgs.br:10183/250315Repositório InstitucionalPUBhttps://lume.ufrgs.br/oai/requestlume@ufrgs.bropendoar:2023-01-14T08:14:46Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false |
dc.title.pt_BR.fl_str_mv |
A3 receptor agonist modulates IL-1β hippocampus levels in a rat model of neuropathic pain |
title |
A3 receptor agonist modulates IL-1β hippocampus levels in a rat model of neuropathic pain |
spellingShingle |
A3 receptor agonist modulates IL-1β hippocampus levels in a rat model of neuropathic pain Cioato, Stefania Giotti Receptor A3 de adenosina Citocinas Dimetil sulfóxido Neuralgia Fatores de crescimento neural Ratos Adenosine A3 receptor Cytokine DMSO N6-(3-iodobenzyl) adenosine-5’-methyluronamide (IB-MECA) Neuropathic pain Neurotrophin Rats |
title_short |
A3 receptor agonist modulates IL-1β hippocampus levels in a rat model of neuropathic pain |
title_full |
A3 receptor agonist modulates IL-1β hippocampus levels in a rat model of neuropathic pain |
title_fullStr |
A3 receptor agonist modulates IL-1β hippocampus levels in a rat model of neuropathic pain |
title_full_unstemmed |
A3 receptor agonist modulates IL-1β hippocampus levels in a rat model of neuropathic pain |
title_sort |
A3 receptor agonist modulates IL-1β hippocampus levels in a rat model of neuropathic pain |
author |
Cioato, Stefania Giotti |
author_facet |
Cioato, Stefania Giotti Medeiros, Liciane Fernandes Lopes, Bettega Costa Medeiros, Helouise Richardt Caumo, Wolnei Roesler, Rafael Torres, Iraci Lucena da Silva |
author_role |
author |
author2 |
Medeiros, Liciane Fernandes Lopes, Bettega Costa Medeiros, Helouise Richardt Caumo, Wolnei Roesler, Rafael Torres, Iraci Lucena da Silva |
author2_role |
author author author author author author |
dc.contributor.author.fl_str_mv |
Cioato, Stefania Giotti Medeiros, Liciane Fernandes Lopes, Bettega Costa Medeiros, Helouise Richardt Caumo, Wolnei Roesler, Rafael Torres, Iraci Lucena da Silva |
dc.subject.por.fl_str_mv |
Receptor A3 de adenosina Citocinas Dimetil sulfóxido Neuralgia Fatores de crescimento neural Ratos |
topic |
Receptor A3 de adenosina Citocinas Dimetil sulfóxido Neuralgia Fatores de crescimento neural Ratos Adenosine A3 receptor Cytokine DMSO N6-(3-iodobenzyl) adenosine-5’-methyluronamide (IB-MECA) Neuropathic pain Neurotrophin Rats |
dc.subject.eng.fl_str_mv |
Adenosine A3 receptor Cytokine DMSO N6-(3-iodobenzyl) adenosine-5’-methyluronamide (IB-MECA) Neuropathic pain Neurotrophin Rats |
description |
Introduction: Considering the lack of specific treatments for neuropathic pain, this study aimed to evaluate the effect of a single dose of adenosine A3 receptor IB-MECA on inflammatory and neurotrophic parameters in rats subjected to a neuropathic pain model. Methods: 64 adult male Wistar rats were used. Neuropathic pain was induced by chronic constriction injury (CCI) of the sciatic nerve and the treatment consisted of a 0.5 μmol/kg dose of IB-MECA, a selective A3 adenosine receptor agonist, dissolved in 3% DMSO; vehicle groups received DMSO 3% in saline solution, and morphine groups received 5 mg/kg. Cerebral cortex and hippocampus IL-1β, BDNF, and NGF levels were determined by Enzyme-Linked Immunosorbent assay. Results: The main outcome was that a single dose of IB-MECA was able to modulate the IL-1β hippocampal levels in neuropathic pain induced by CCI and the DMSO increased IL-1β and NGF hippocampal levels in sham-operated rats. However, we did not observe this effect when the DMSO was used as vehicle for IB-MECA, indicating that IB-MECA was able to prevent the effect of DMSO. Conclusions: Considering that the IL-1β role in neuropathic pain and the contributions of the hippocampus are well explored, our result corroborates the relationship between the A3 receptor and the process of chronic pain maintenance. |
publishDate |
2022 |
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2022-10-26T04:47:33Z |
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2022 |
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http://hdl.handle.net/10183/250315 |
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2357-9730 |
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001148411 |
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dc.relation.ispartof.pt_BR.fl_str_mv |
Clinical and biomedical research. Porto Alegre. Vol. 42, no. 2 (2022), p. 128-134 |
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